Oral Manifestations of Disease¶
Chapter 38 | Part 2: Cardinal Manifestations and Presentation of Diseases · Part 2 – Cardinal Manifestations & Presentation · Chapter 38
Key Clinical Points¶
- Laryngitis is typically self-limited (3–7 days) but may persist up to 14 days; antibiotics are not indicated for uncomplicated cases.
- Dental caries progress from enamel → dentin → pulp → necrosis/abscess; Streptococcus mutans is the primary pathogen.
- Periodontal disease is a major cause of tooth loss and is linked to systemic conditions including coronary heart disease and stroke.
- Pathognomonic signs: 'strawberry gums' (granulomatosis with polyangiitis), 'target' lesions (erythema multiforme major), Hutchinson's incisors/mulberry molars (congenital syphilis).
- High-risk sites for oral cancer: lower lip, floor of the mouth, ventral tongue, and soft palate.
- Drug-induced gingival overgrowth (e.g., from calcium channel blockers) may be reversed upon drug discontinuation.
- Oral melanoma is aggressive, expanding/invading early; benign nevi typically remain stable.
- Persistent oral lesions (>2 weeks) or mixed red/white patches require biopsy to rule out squamous cell carcinoma.
- Acute necrotizing ulcerative gingivitis (NUG) presents with sudden inflammation, ulceration, bleeding, and fetid halitosis.
- Specific tongue alterations (e.g., hairy tongue, bald tongue) can indicate systemic conditions like HIV, nutritional deficiencies, or fungal infections.
DEFINITION & OVERVIEW¶
• Scope: Includes conditions of the larynx, teeth, periodontium, and oral mucosa. These may be primary oral diseases or secondary manifestations of systemic conditions. • Laryngitis: Characterized by a raspy, hoarse, or breathy voice; associated with dry cough and anterior throat pain; patients often feel a need to clear their throats. • Teeth & Periodontal Structures: ◦ Development: Begins at 6 weeks of embryonic life → continues through age 17. ◦ Structure: Crown (enamel) + Root (covered by bone-like cementum). ◦ Composition: Dentin forms the majority of the tooth substance; pulp contains vascular and nerve supply. ◦ Support: Periodontium includes gingivae, alveolar bone, cementum, and periodontal ligament. • Oral Mucosa: Most diseases involve microorganisms. Ulceration is the most common oral mucosal lesion.
EPIDEMIOLOGY¶
• Dental/Periodontal Disease: Major global public health problem despite local improvements from fluoridation and improved care. ◦ High-risk groups: Hyposalivation/xerostomia, diabetics, alcoholics, tobacco users, Down syndrome, and those with gingival hyperplasia. ◦ Access issues: Low socioeconomic status or limited self-care (disabilities, elderly, dementia) increase risk. • Oral Cancer Risk Factors: ◦ Western countries: Sun exposure (lower lip), tobacco/alcohol use, and human papillomavirus (HPV) infection. ◦ Asia/India: Smokeless tobacco mixed with betel nut, slaked lime, and spices.
ETIOLOGY & PATHOPHYSIOLOGY¶
• Dental Caries Pathogenesis: ◦ Process: Bacteria (primarily Streptococcus mutans) → colonize organic buffering biofilm (plaque) → produce acids → demineralize enamel. ◦ Sites: Fissures/pits (early), then dentin → pulp → acute pulpitis. • Periodontal Disease Pathogenesis: ◦ Process: Plaque → Calculus (calcified plaque) → Chronic inflammation → Gingivitis (hyperemia, bleeding) → Periodontitis (sulcus deepening, ligament destruction, bone loss). • Mucosal Disease Etiology: ◦ Infections: Viral (HSV, VZV, EBV, Coxsackievirus), Bacterial (Syphilis, Gonorrhea, Tuberculosis, Actinomycosis), Fungal (Candidiasis, Histoplasmosis). ◦ Other: Dermatologic (Pemphigoid, Pemphigus, Lichen planus, Erythema multiforme), Traumatic, Squamous cell carcinoma (SCC), Leukemia, Lymphoma.
CLINICAL FEATURES¶
• Laryngitis: ◦ Symptoms: Raspy/hoarse voice, dry cough, anterior throat pain. ◦ Exam: Diagnosis usually based on history; if visualized (mirror or flexible laryngoscopy), shows erythema and edema of the vocal cords.
Dental & Periodontal Features¶
• Pulpal Disease: ◦ Pulpitis: Severe, sharp/throbbing pain → worse when lying down. ◦ Necrosis: Loss of cold sensitivity; pain becomes constant or intermittent. ◦ Periapical complications: ◦ Granuloma/Cyst → radiolucency at root apex. ◦ Abscess → can lead to osteomyelitis, parulis (gum boil), or virulent cellulitis (Ludwig's angina) in submandibular space/floor of mouth. • Periodontal Disease: ◦ Gingivitis: Bleeding with brushing. ◦ Periodontitis: Deepening sulcus, tissue destruction, and tooth loosening. ◦ Acute Necrotizing Ulcerative Gingivitis (NUG): Sudden inflammation, ulceration, bleeding, and fetid halitosis. ◦ Linear Gingival Erythema: Associated with advanced HIV/reduced neutrophil activity.
Mucosal & Pigmented Lesions¶
• Ulcerative Lesions: ◦ Acute: Usually painful and self-limited (e.g., aphthae, HSV). ◦ Chronic/Suspicious: Painless ulcers or mixed red/white patches (>2 weeks) → suspect SCC or premalignant dysplasia. ◦ Specific conditions: ◦ Aphthous ulcers: Common in Behçet's syndrome; seen in reactive arthritis, SLE, and Crohn's disease (granulomatous). ◦ Celiac Disease: Higher prevalence of recurrent aphthae → may remit with gluten removal. • Pigmented Lesions: ◦ Melanotic macule/Nevi: Stable, no growth. ◦ Malignant melanoma: Can be flat or nodular; expands and invades early. ◦ Systemic markers: ◦ Addison's: Bluish-black spots + skin pigmentation. ◦ Peutz-Jeghers: Dark-brown spots on lips/mucosa + intestinal polyposis. ◦ Other: Amalgam tattoo (blue-black, radiopaque), Heavy metal (thin line at gingival margin; bismuth, mercury, lead), Fordyce spots (yellow, sebaceous glands), Kaposi's sarcoma (red/blue plaques).
White Lesions & Tongue Alterations¶
• White Lesions: ◦ Lichen planus: Striae, white plaques, red areas; purplish papules on skin. ◦ Smoker's leukoplakia: White patch (firm/rough); 2% risk of SCC → biopsy essential. ◦ Erythroplakia: Velvety, reddish plaque; high risk for malignancy. ◦ Candidiasis: ◦ Pseudomembranous ('thrush'): Creamy white curdlike patches → raw surface when scraped. ◦ Erythematous: Flat, red, sometimes sore areas. ◦ Candidal leukoplakia: Nonremovable white thickening of epithelium. ◦ Hairy leukoplakia: White areas on vertical folds; associated with HIV. ◦ Warts (HPV): Papillary lesions with thick, white surfaces. • Tongue Alterations: ◦ Macroglossia: Enlarged tongue → syndromes (Down, Beckwith-Wiedemann), tumors, or metabolic/endocrine issues. ◦ Hairy tongue: Elongated filiform papillae; stained by tobacco/food/bacteria. ◦ Bald tongue: Atrophy from xerostomia, anemia, pellagra, or syphilis; may be erythematous candidiasis. ◦ Median rhomboid glossitis: Ovoid, denuded area in posterior tongue → congenital; may respond to antifungals.
DIFFERENTIAL DIAGNOSIS¶
• Ulcerative Lesions (Table 38-1): ◦ Viral: ◦ Primary herpetic gingivostomatitis (HSV 1/2): Painful, vesicles → ulcerate; infants/children. ◦ Recurrent herpes labialis: Mucocutaneous junction; painful to pressure. ◦ Recurrent intraoral herpes: Palate/gingiva; small vesicles on keratinized tissue. ◦ Chickenpox (VZV): Gingiva/mucosa; may form large bullous lesions. ◦ Herpes zoster (VZV): Unilateral, linear pattern along trigeminal nerve. ◦ Infectious mononucleosis (EBV): Fatigue, sore throat; petechiae on palate. ◦ Herpangina (Coxsackievirus A/B/Echovirus): Sudden fever, pharyngeal vesicles (children <4). ◦ Hand-foot-and-mouth (Coxsackievirus A16): Fever, malaise; kids <10. ◦ Primary HIV: Acute gingivitis/ulceration → febrile illness resembling mononucleosis. ◦ Bacterial/Fungal/Other: ◦ NUG: Painful, bleeding gingiva; necrosis of papillae; foul breath. ◦ Syphilis (Congenital): Hutchinson's incisors, mulberry molars, gummatous palate. ◦ Syphilis (Primary): Chancre; painless ulcer with indurated border. ◦ Syphilis (Secondary): Mucous patches on palate/commissures; maculopapular lesions. ◦ Syphilis (Tertiary): Gummatous infiltration → bald tongue. ◦ Gonorrhea: Pharyngitis; may be asymptomatic or produce burning sensation. ◦ Tuberculosis: Painless, solitary ulcer with firm undermined border. ◦ Actinomycosis: Swellings of face/neck; 'sulfur granules'. ◦ Histoplasmosis: Nodulous, verrucous, or granulomatous lesions. ◦ Mucous membrane pemphigoid: Gingival erythema and ulceration. ◦ Erythema multiforme major: Target lesions; rapid onset. ◦ Squamous cell carcinoma (SCC): Red/white/mixed; fails to heal; invasive. ◦ Acute myeloid leukemia (Monocytic): Gingival swelling → hyperpigmentation → hemorrhage. ◦ Lymphoma: Rapidly proliferating ulcerated area. ◦ Burns: White slough from corrosive agents or heat.
DIAGNOSTIC APPROACH¶
- Laryngitis:
- Primary assessment: Clinical history (voice quality, cough duration).
- If needed: Indirect examination with mirror or flexible laryngoscopy → identify erythema/edema.
- Dental & Periodontal:
- Clinical exam of gingiva and teeth.
- Radiography: Identify periapical radiolucency (granuloma/cyst) or bone loss.
- Mucosal Lesions:
- Visual inspection for color, size, and duration.
- Biopsy: Required for any persistent (>2 weeks), non-healing, or suspicious white/red patches to rule out SCC.
MANAGEMENT & TREATMENT¶
- Laryngitis:
- Supportive care for symptoms.
- Note: Antibiotics not required for uncomplicated cases.
- Dental Caries/Pulpal Disease:
- Removal of decay → restoration or extraction.
- Periodontal Disease:
- Professional cleaning and scaling.
- Oral hygiene education.
- Mucosal Lesions:
- Topical steroids for inflammatory conditions (e.g., Lichen planus).
- Antifungals for Candidiasis.
- Referral/Biopsy for suspected malignancy.
- Systemic Management:
- Treat underlying causes (e.g., steroid replacement for Addison's, ART for HIV).
PROGNOSIS & COMPLICATIONS¶
• Laryngitis: Generally self-limited; complications rare in uncomplicated cases. • Malignancy (SCC/Melanoma): ◦ SCC: Invades tissue, metastasizes to regional nodes → poor prognosis if late detection. ◦ Melanoma: Rapid expansion and early metastasis → high mortality risk. • Periodontal Complications: ◦ Loss of teeth; systemic links to coronary heart disease and stroke.
SPECIAL CONSIDERATIONS¶
• Pregnancy: (General clinical caution for oral medications). • HIV/AIDS (Table 38-5): ◦ Papules, nodules, plaques: Candidiasis, Condyloma acuminatum, SCC, Non-Hodgkin's lymphoma, Hairy leukoplakia. ◦ Pigmented lesions: Kaposi's sarcoma, Bacillary angiomatosis, Zidovudine pigmentation, Addison's disease. • Diabetes: Increased risk for periodontal disease and candidiasis. • Drug Interactions/Effects: ◦ Calcium channel blockers → Gingival overgrowth. ◦ Neuroleptics/Zidovudine → Pigmentation.
KEY PEARLS & CLINICAL TRAPS¶
• Pathognomonic Clues: → Strawberry gums = Granulomatosis with polyangiitis. → Target lesions = Erythema multiforme major. → Hutchinson's incisors/Mulberry molars = Congenital syphilis. • Clinical Traps: → Do not assume all oral ulcers are minor; any lesion >2 weeks requires biopsy. → Distinguish between stable pigmented macules and invasive melanomas. → Recognize 'trench mouth' (NUG) as a rapid, severe infection requiring debridement.
Reference Tables¶
TABLE 38-1 Vesicular, Bullous, or Ulcerative Lesions of the Oral Mucosa CONDITION Viral Diseases Primary acute herpetic…¶
Harrison's 22e, p.262
| CONDITION | USUAL LOCATION | CLINICAL FEATURES | COURSE |
|---|---|---|---|
| Viral Diseases | |||
| Primary acute herpetic gingivostomatitis (HSV type 1; rarely type 2) |
Lip and oral mucosa (buccal, gingival, lingual mucosa) |
Labial vesicles that rupture and crust, and intraoral vesicles that quickly ulcerate; extremely painful; acute gingivitis, fever, malaise, foul odor, and cervical lymphadenopathy; occurs primarily in infants, children, and young adults |
Heals spontaneously in 10–14 days; unless secondarily infected, lesions lasting >3 weeks are not due to primary HSV infection |
| Mucocutaneous junction of lip, perioral skin |
Eruption of groups of vesicles that may coalesce, then rupture and crust; painful to pressure or spicy foods |
||
| Recurrent intraoral herpes simplex |
Palate and gingiva | Small vesicles on keratinized epithelium that rupture and coalesce; painful |
Heals spontaneously in ∼1 week; if severe, topical or oral antiviral treatment may reduce healing time |
| Gingiva and oral mucosa |
Skin lesions may be accompanied by small vesicles on oral mucosa that rupture to form shallow ulcers; may coalesce to form large bullous lesions that ulcerate; mucosa may have generalized erythema |
||
| Herpes zoster (VZV reactivation) |
Cheek, tongue, gingiva, or palate |
Unilateral vesicular eruptions and ulceration in linear pattern following sensory distribution of trigeminal nerve or one of its branches |
Gradual healing without scarring unless secondarily infected; postherpetic neuralgia is common; oral acyclovir, famciclovir, or valacyclovir reduces healing time and postherpetic neuralgia |
| Oral mucosa | Fatigue, sore throat, malaise, fever, and cervical lymphadenopathy; numerous small ulcers usually appear several days before lymphadenopathy; gingival bleeding and multiple petechiae at junction of hard and soft palates |
||
| Herpangina (coxsackievirus A; also possibly coxsackievirus B and echovirus) |
Oral mucosa, pharynx, tongue |
Sudden onset of fever, sore throat, and oropharyngeal vesicles, usually in children <4 years old, during summer months; diffuse pharyngeal congestion and vesicles (1–2 mm), grayish-white surrounded by red areola; vesicles enlarge and ulcerate |
Incubation period of 2–9 days; fever for 1–4 days; recovery uneventful |
| Oral mucosa, pharynx, palms, and soles |
Fever, malaise, headache with oropharyngeal vesicles that become painful, shallow ulcers; highly infectious; usually affects children under age 10 |
||
| Primary HIV infection | Gingiva, palate, and pharynx |
Acute gingivitis and oropharyngeal ulceration, associated with febrile illness resembling mononucleosis and including lymphadenopathy |
Followed by HIV seroconversion, asymptomatic HIV infection, and usually ultimately by HIV disease |
| Bacterial or Fungal Diseases | |||
| Gingiva | Painful, bleeding gingiva characterized by necrosis and ulceration of gingival papillae and margins plus lymphadenopathy and foul breath |
||
| Prenatal (congenital) syphilis |
Palate, jaws, tongue, and teeth |
Gummatous involvement of palate, jaws, and facial bones; Hutchinson’s incisors, mulberry molars, glossitis, mucous patches, and fissures at corner of mouth |
Tooth deformities in permanent dentition irreversible |
| Lesion appearing where organism enters body; may occur on lips, tongue, or tonsillar area |
Small papule developing rapidly into a large, painless ulcer with indurated border; unilateral lymphadenopathy; chancre and lymph nodes containing spirochetes; serologic tests positive by third to fourth weeks |
||
| Secondary syphilis | Oral mucosa frequently involved with mucous patches, which occur primarily on palate and also at commissures of mouth |
Maculopapular lesions of oral mucosa, 5–10 mm in diameter with central ulceration covered by grayish membrane; eruptions occurring on various mucosal surfaces and skin, accompanied by fever, malaise, and sore throat |
Lesions may persist from several weeks to a year |
| Palate and tongue | Gummatous infiltration of palate or tongue followed by ulceration and fibrosis; atrophy of tongue papillae produces characteristic bald tongue and glossitis |
||
| Gonorrhea | Lesions may occur in mouth at site of inoculation or secondarily by hematogenous spread from a primary focus |
Most pharyngeal infection is asymptomatic; may produce burning or itching sensation; oropharynx and tonsils may be ulcerated and erythematous; saliva viscous and fetid |
More difficult to eradicate than urogenital infection, though pharyngitis usually resolves with appropriate antimicrobial treatment |
| Tongue, tonsillar area, soft palate |
Painless, solitary, 1- to 5-cm, irregular ulcer covered with persistent exudate; ulcer has firm undermined border |
||
| Cervicofacial actinomycosis |
Swellings in region of face, neck, and floor of mouth |
Infection may be associated with extraction, jaw fracture, or eruption of molar tooth; in acute form, resembles acute pyogenic abscess, but contains yellow “sulfur granules” (gram-positive mycelia and their hyphae) |
Typically, swelling is hard and grows painlessly; multiple abscesses with draining tracts develop; penicillin first choice; surgery usually necessary |
TABLE 38-2 Pigmented Lesions of the Oral Mucosa CONDITION Oral melanotic macule Diffuse melanin pigmentation Nevi…¶
Harrison's 22e, p.264
| CONDITION | USUAL LOCATION | CLINICAL FEATURES | COURSE |
|---|---|---|---|
| Oral melanotic macule | Any area of mouth | Discrete or diffuse, localized, brown to black macule | Remains indefinitely; no growth |
| Any area of mouth | Diffuse pale to dark-brown pigmentation; may be physiologic (“racial”) or due to smoking |
||
| Nevi | Any area of mouth | Discrete, localized, brown to black pigmentation | Remains indefinitely |
| Any area of mouth | Can be flat and diffuse, painless, brown to black; or can be raised and nodular |
||
| Addison’s disease | Any area of mouth, but mostly buccal mucosa |
Blotches or spots of bluish-black to dark-brown pigmentation occurring early in disease, accompanied by diffuse pigmentation of skin; other symptoms of adrenal insufficiency |
Condition controlled by adrenal steroid replacement |
| Any area of mouth | Dark-brown spots on lips, buccal mucosa, with characteristic distribution of pigment around lips, nose, and eyes and on hands; concomitant intestinal polyposis |
||
| Drug ingestion (neuroleptics, oral contraceptives, minocycline, zidovudine, quinine derivatives) |
Any area of mouth | Brown, black, or gray areas of pigmentation | Gradually disappears following cessation of drug intake |
| Gingiva and alveolar mucosa |
Small blue-black pigmented areas associated with embedded amalgam particles in soft tissues; may show up on radiographs as radiopaque particles in some cases |
||
| Heavy metal pigmentation (bismuth, mercury, lead) |
Gingival margin | Thin blue-black pigmented line along gingival margin; rarely seen except in children exposed to lead-based paint |
Indicative of systemic absorption; no significance for oral health |
| Dorsum of tongue | Elongation of filiform papillae of tongue, which become stained by coffee, tea, tobacco, or pigmented bacteria |
||
| Fordyce spots | Buccal and labial mucosa | Numerous small yellowish spots just beneath mucosal surface; no symptoms; due to hyperplasia of sebaceous glands |
Benign; remains without apparent change |
| Palate most common, but may occur at any other site |
Red or blue plaques of variable size and shape; often enlarge, become nodular, and may ulcerate |
||
| Mucous retention cysts | Buccal and labial mucosa | Bluish, clear fluid–filled cyst due to extravasated mucus from injured minor salivary gland |
Benign; painless unless traumatized; may be removed surgically |
TABLE 38-3 White Lesions of Oral Mucosa CONDITION Lichen planus¶
Harrison's 22e, p.264
| CONDITION | USUAL LOCATION | CLINICAL FEATURES | COURSE |
|---|---|---|---|
| Lichen planus | Buccal mucosa, tongue, gingiva, and lips; skin |
Striae, white plaques, red areas, ulcers in mouth; purplish papules on skin; may be asymptomatic, sore, or painful; lichenoid drug reactions may look similar |
Protracted; responds to topical glucocorticoids |
| Oral mucosa, vagina, anal mucosa |
Painless white thickening of epithelium; adolescence/early adulthood onset; familial |
||
| Smoker’s leukoplakia and smokeless tobacco lesions |
Any area of oral mucosa, sometimes related to location of habit |
White patch that may become firm, rough, or red-fissured and ulcerated; may become sore and painful but is usually painless |
May or may not resolve with cessation of habit; 2% of patients develop squamous cell carcinoma; early biopsy essential |
| Floor of mouth commonly affected in men; tongue and buccal mucosa in women |
Velvety, reddish plaque; occasionally mixed with white patches or smooth red areas |
||
| Candidiasis | Any area in mouth | Pseudomembranous type (“thrush”): creamy white curdlike patches that reveal a raw, bleeding surface when scraped; found in sick infants, debilitated elderly patients receiving high-dose glucocorticoids or broad-spectrum antibiotics, and patients with AIDS |
Responds favorably to antifungal therapy and correction of predisposing causes where possible |
| Erythematous type: flat, red, sometimes sore areas in same groups of patients |
Course same as for pseudomembranous type | ||
| Candidal leukoplakia: nonremovable white thickening of epithelium due to Candida |
Responds to prolonged antifungal therapy | ||
| Angular cheilitis: sore fissures at corner of mouth | Responds to topical antifungal therapy | ||
| Usually on lateral tongue, rarely elsewhere on oral mucosa |
White areas ranging from small and flat to extensive accentuation of vertical folds; found in HIV carriers (all risk groups for AIDS) |
||
| Warts (human papillomavirus) |
Anywhere on skin and oral mucosa |
Single or multiple papillary lesions with thick, white, keratinized surfaces containing many pointed projections; cauliflower lesions covered with normal-colored mucosa or multiple pink or pale bumps (focal epithelial hyperplasia) |
Lesions grow rapidly and spread; squamous cell carcinoma must be ruled out with biopsy; excision or laser therapy; may regress in HIV-infected patients receiving antiretroviral therapy |
TABLE 38-5 Oral Lesions Associated with HIV Infection¶
Harrison's 22e, p.265
| TYPE OF CHANGE | CLINICAL FEATURES |
|---|---|
| Size or Morphology | |
| Macroglossia | Enlarged tongue that may be part of a syndrome found in developmental conditions such as Down syndrome, Simpson-Golabi-Behmel syndrome, or Beckwith-Wiedemann syndrome; may be due to tumor (hemangioma or lymphangioma), metabolic disease (e.g., primary amyloidosis), or endocrine disturbance (e.g., acromegaly or cretinism); may occur when all teeth are removed |
TABLE 38-5 Oral Lesions Associated with HIV Infection
| LESION MORPHOLOGY | ETIOLOGIES |
|---|---|
| Papules, nodules, plaques | Candidiasis (hyperplastic and pseudomembranous)a Condyloma acuminatum (human papillomavirus infection) Squamous cell carcinoma (preinvasive and invasive) Non-Hodgkin’s lymphomaa Hairy leukoplakiaa |
| Median rhomboid glossitis | Congenital abnormality with ovoid, denuded area in median posterior portion of tongue; may be associated with candidiasis and may respond to antifungal treatment |
| Color | |
| Hairy tongue | Elongation of filiform papillae of medial dorsal surface area due to failure of keratin layer of papillae to desquamate normally; brownish-black coloration may be due to staining by tobacco, food, or chromogenic organisms |
| Pigmented lesions | Kaposi’s sarcomaa Bacillary angiomatosis (skin and visceral lesions more common than oral) Zidovudine pigmentation (skin, nails, and occasionally oral mucosa) Addison’s disease |
| “Bald” tongue | Atrophy may be associated with xerostomia, pernicious anemia, iron-deficiency anemia, pellagra, or syphilis; may be accompanied by painful burning sensation; may be an expression of erythematous candidiasis and respond to antifungal treatment |